المؤلفون: Yuhan, Zhu, Jingyuan, Zhang, Xiaofeng, Yao, Tianming, Qiu, Liping, Jiang, Ningning, Wang, Yan, Shi, Chenbing, Wu, Weizhuo, Yuan, Guang, Yang, Xiaofang, Liu, Jie, Bai, Lili, Men, Xiance, Sun

المصدر: Food and Chemical Toxicology. 160:112771

مصطلحات موضوعية: Male, Pore Forming Cytotoxic Proteins, Arsenites, Ubiquitination, General Medicine, Phosphate-Binding Proteins, Toxicology, Sodium Compounds, Cell Line, Rats, Rats, Sprague-Dawley, Liver, NLR Family, Pyrin Domain-Containing 3 Protein, Hepatocytes, Pyroptosis, Animals, Humans, Insulin Resistance, Food Science

الوصف: As an environmental toxicant, arsenic exposure may cause insulin resistance (IR). Previous studies have shown that pyroptosis plays an important role in the occurrence and development of IR. Although gasdermin D (GSDMD) functions as an executor of pyroptosis, the relationship between GSDMD-mediated pyroptosis and hepatic IR remains unclear. Here, we observed that sodium arsenite (NaAsO

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::735fb184bdef1ad96575515e3936262aTest
https://doi.org/10.1016/j.fct.2021.112771Test

المؤلفون: Chengyan Geng, Qiujuan Li, Xiaofeng Yao, Liping Jiang, Zeyun Gao, Yong Liu, Xiaoxia Shi, Xuan Wang, Jun Cao, Zhiguo Li

المصدر: Toxicology in vitro : an international journal published in association with BIBRA. 66

مصطلحات موضوعية: 0301 basic medicine, Cell Survival, ATG5, Autophagy-Related Proteins, Toxicology, Autophagy-Related Protein 5, Cell Line, 03 medical and health sciences, 0302 clinical medicine, Adenosine Triphosphate, Autophagy, Humans, Glycolysis, Lactic Acid, Cell Proliferation, A549 cell, Chemistry, Cell growth, Cell Cycle, General Medicine, Transfection, Cell cycle, Cell biology, Cysteine Endopeptidases, 030104 developmental biology, Glucose, Anaerobic glycolysis, 030220 oncology & carcinogenesis, Cadmium

الوصف: Cadmium (Cd) is a pervasive harmful metal in the environment. It is a well-known inducer of tumorigenesis, but its mechanism is still unclear. We have previously reported that Cd-induced autophagy was apoptosis-dependent and prevents apoptotic cell death to ensure the growth of A549 cells. In this study, the mechanism was further investigated. Cd treatment increased glucose uptake and lactate release significantly. Meanwhile, the protein level of GLUT1，HKII，PKM2 and LDHA increased in a time-dependent manner, indicating that Cd induced aerobic glycolysis in A549 and HELF cells. The inhibitors of autophagy, 3MA, and CQ, repressed Cd-induced glycolysis-related proteins, indicating that autophagy was involved in Cd-induced glycolysis in A549 and HELF cells. Knockdown of ATG4B or ATG5 by siATG4B and siATG5 decreased Cd-induced glycolysis, while overexpression of ATG4B enhanced glycolysis. These results demonstrated that Cd-induced glycolysis was autophagy-dependent. Then, glycolysis inhibitor, 2DG and siPKM2 could inhibit Cd-induced cell viability and cell cycle progression compared to only Cd treatment, indicating that glycolysis played an important role in Cd-induced cell growth. Finally, co-treatment of transfection of ATG4B-DNA plasmids with 2DG or siPKM2 further demonstrated that the autophagy-glycolysis axis played an important role in Cd-induced cell cycle progression. Taken together, our results suggested that Cd-induced glycolysis is autophagy-dependent and the autophagy-glycolysis axis underlies the mechanism of Cd-induced cell growth in A549 and HELF cells.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fbbf1aea4bde2a61bb0478037340cedbTest
https://pubmed.ncbi.nlm.nih.gov/32200033Test

المؤلفون: Zhidong, Wang, Ye, Tao, Tianming, Qiu, Xiaofeng, Yao, Liping, Jiang, Ningning, Wang, Sen, Wei, Xue, Jia, Pei, Pei, Guang, Yang, Xiaofang, Liu, Shuang, Liu, Xiance, Sun

المصدر: Chemico-biological interactions. 300

مصطلحات موضوعية: Cell Survival, Taurine, RNA-Binding Proteins, Cell Line, Mice, Inbred C57BL, Mice, Arsenic Trioxide, Liver, Autophagy, Hepatic Stellate Cells, Animals, Humans, PPAR alpha, Microtubule-Associated Proteins

الوصف: The activation of hepatic stellate cells (HSCs) is a key event in the development of hepatic fibrosis caused by arsenic. However, it is unclear how arsenic induces the activation of HSCs. In the present study, we found that arsenic trioxide (As

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=pmid________::70f8ca006914f657b12b4143652da784Test
https://pubmed.ncbi.nlm.nih.gov/30677399Test

المؤلفون: Xiaofang Liu, Shaopeng Wang, Liping Jiang, Nairong Liu, Yueran Bai, Xiance Sun, Guang Yang, Xiaofeng Yao, Xingyue Zhai, Xueyan Wu

المصدر: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 106

مصطلحات موضوعية: 0301 basic medicine, Cell Survival, Caspase 3, Apoptosis, Mitochondrion, Toxicology, Cathepsin B, Cell Line, 03 medical and health sciences, Diethylhexyl Phthalate, Autophagy, Humans, Cathepsin, Membrane Potential, Mitochondrial, TUNEL assay, biology, Cytochrome c, Cytochromes c, Endothelial Cells, General Medicine, Cell biology, Mitochondria, 030104 developmental biology, biology.protein, Lysosomes, Food Science

الوصف: Mono(2-ethylhexyl) phthalate (MEHP), the active metabolite of di(2-ethylhexyl) phthalate (DEHP), has been known to have adverse effects on the reproductive system, urologic systems, hepatic, developmental toxicities and carcinogenicity. However, the effect of MEHP on cardiovascular toxicity remains unclear. Therefore, we aimed to evaluate the cytotoxic effects of MEHP and the possible molecular mechanism. We found that treatment of EA.hy 926 cells with MEHP induced autophagy at earlier time (6 h) in this study. Lysosomal membrane permeabilization (LMP) occurred, after treatment with MEHP for 12 h, followed by the release of cathepsin B. Autophagy inhibitor 3-methyladenine (3MA) attenuated MEHP-induced LMP and the release of cathepsin B in EA.hy 926 cells. Additionally, MEHP induced collapse of mitochondrial transmembrane potential, which was evidenced by JC-1 staining. Addition of 3MA relieved MEHP-induced apoptosis as assessed by the expression of caspase 3 and TUNEL assay, indicating that MEHP-induced apoptosis was autophagy-dependent. Cathepsin B inhibitor, CA-074 Me, suppressed MEHP-induced the mitochondria release of cytochrome c and apoptosis as well. In summary, our results suggest that MEHP induced autophagy-dependent apoptosis in EA.hy 926 cells through the lysosomal-mitochondrial axis. This study provides new mechanistic insights into MEHP-induced cardiovascular toxicity.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c192c5b41bbb558efbe9d4a304e71760Test
https://pubmed.ncbi.nlm.nih.gov/28579546Test

المؤلفون: Xiance Sun, Xingyue Zhai, Xiaofeng Yao, Guang Yang, Xueyan Wu, Yueran Bai, Xiaofang Liu, Shaopeng Wang, Liping Jiang, Nairong Liu

المصدر: Toxicology in vitro : an international journal published in association with BIBRA. 44

مصطلحات موضوعية: 0301 basic medicine, Autophagosome, Programmed cell death, Cell Survival, Biology, Toxicology, Cell Line, 03 medical and health sciences, Western blot, Diethylhexyl Phthalate, medicine, Autophagy, Humans, Viability assay, RNA, Small Interfering, Cytotoxicity, chemistry.chemical_classification, Membrane Potential, Mitochondrial, Sirolimus, Reactive oxygen species, medicine.diagnostic_test, Activator (genetics), Adenine, Endothelial Cells, General Medicine, Cell biology, Acetylcysteine, 030104 developmental biology, chemistry, embryonic structures, Reactive Oxygen Species, Microtubule-Associated Proteins, Proto-Oncogene Proteins c-akt

الوصف: Mono-(2-ethylhexyl) phthalate (MEHP) is an active metabolite of di-(2-ethylhexyl) phthalate (DEHP). MEHP has toxic effects on cardiovascular system, but the possible molecular mechanisms are not completely elucidated. In our study, 3-methyladenine (3-MA), an autophagosome formation inhibitor, protected the EA.hy926 cells against MEHP cytotoxicity, and rapamycin, an autophagosome formation stimulator, further decreased the cell viability in the MEHP-treated EA.hy926 cells. Thus, autophagy may play an important role in MEHP-induced toxicity. MEHP increased the autophagosome number in EA.hy926 cells detected under transmission electron microscope. Collapses of ΔΨm and reactive oxygen species (ROS) level were increased in a dose-dependent manner under treatment with 0-200μM MEHP for 24h. N-acetyl-l-cysteine (NAC), a ROS inhibitor, protected against MEHP-induced cytotoxicity and decreased the protein expression of LC3-II. These findings suggested that MEHP-induced autophagic cell death was ROS-dependent in EA.hy926 cells. Knockdown of Akt1 with Akt1 siRNA aggravated MEHP-induced cell death, and insulin, an Akt1 activator, alleviated MEHP-induced cell death. These results were consistent with the expression of LC3-II using western blot. The phospho-Akt1(Ser473) (p-Akt1) level was enhanced after pretreatment with NAC. In conclusion, it is possible that ROS elicited autophagy through Akt1 pathway in the MEHP-treated EA.hy926 cells.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::74131d942e3ff58e01846c3971709d2aTest
https://pubmed.ncbi.nlm.nih.gov/28655635Test

المؤلفون: Chengyan Geng, Jun Cao, Xiang Xin Xue, Xiaomei Zhang, Liping Jiang, Xiaofeng Yao, Laifu Zhong

المصدر: Journal of Trace Elements in Medicine and Biology. 22:189-195

مصطلحات موضوعية: Lipopolysaccharides, Antioxidant, Lipopolysaccharide, medicine.medical_treatment, Inflammation, Pharmacology, medicine.disease_cause, Biochemistry, Monocytes, Cell Line, Inorganic Chemistry, chemistry.chemical_compound, Boric Acids, medicine, Humans, Secretion, RNA, Messenger, Sulfhydryl Compounds, Buthionine Sulfoximine, Tumor Necrosis Factor-alpha, Chemistry, Glutathione, Acetylcysteine, Gene Expression Regulation, Molecular Medicine, Tumor necrosis factor alpha, medicine.symptom, Oxidative stress, Intracellular

الوصف: Oxidative stress plays an important role during inflammatory diseases and antioxidant administration to diminish oxidative stress may arrest inflammatory processes. Boron has been implicated to modulate certain inflammatory mediators and regulate inflammatory processes. Here we investigated the role of the tripeptide glutathione (GSH) in modulating the effects of boric acid (BA) on lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) formation in THP-1 monocytes. Interestingly, we found that BA had no significant effects on both TNF-alpha production and intracellular GSH contents, whereas it could inhibit LPS-induced TNF-alpha formation and ameliorated the d,l-buthionine-S,R-sulfoximine (BSO)-induced GSH depletion. Twenty-four hour incubation with BSO induced a decrease of the intracellular GSH and an increase of TNF-alpha. Treatment with N-acetyl-l-cysteine (NAC) did not significantly increase intracellular content of GSH but significantly reduced the secretion of TNF-alpha. BSO-pretreatment for 24h enhanced the LPS-induced secretion and mRNA expression of TNF-alpha further. BA inhibited LPS-stimulated TNF-alpha formation was also seen after GSH depletion by BSO. These results indicate that BA may have anti-inflammatory effect in the LPS-stimulated inflammation and the effect of BA on TNF-alpha secretion may be induced via a thiol-dependent mechanism.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b312266ad9b1957250a299e7c1b4a9e9Test
https://doi.org/10.1016/j.jtemb.2008.03.005Test